Propofol Inhibits Lipopolysaccharide-Induced Tumor Necrosis Factor-Alpha Expression and Myocardial Depression through Decreasing the Generation of Superoxide Anion in Cardiomyocytes
Figure 5
The inhibitory effect of propofol on NADPH oxidase/TNF-α signal pathway in LPS-stimulated myocardium of wild type C57BL/6 mice. Wild type C57BL/6 mice were divided into four groups: control group, propofol alone group, LPS group, and LPS + propofol group. (a) The effect of propofol on gp91phox protein expression in myocardium 2 hours after LPS treatment. (b) Gray intensity analysis of the western blot results of gp91phox expression. (c) The effect of propofol on ERK1/2 phosphorylation in myocardium 1 hour after LPS treatment. (d) Gray intensity analysis of the western blot results of ERK1/2 phosphorylation. (e) The effect of propofol on p38 phosphorylation in myocardium 1 hour after LPS treatment. (f) Gray intensity analysis of the western blot results of p38 phosphorylation. (g) TNF-α protein measurement in myocardium by ELISA at 4 hours after LPS treatment; (h) TNF-α mRNA measurement in myocardium by real time RT-PCR at 2 hours after LPS treatment (each bar represents the mean ± S.D, , compared with LPS group; ).
